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Gene. 2019 Aug 20;710:193-201. doi: 10.1016/j.gene.2019.06.009. Epub 2019 Jun 7.

Long non-coding RNA DILC suppresses bladder cancer cells progression.

Author information

1
Department of Urology surgery, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China.
2
Department of Rehabilitation Medicine, First Affiliated Hospital of Second Military Medical University, Shanghai, 200433, China.
3
Department of Breast and Thyroid surgery, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China.
4
Department of Internal Medicine, The No. 313 Hospital of PLA, Huludao 125000, China.
5
Department of Internal Medicine, First Affiliated Hospital of JinZhou Medical University, JinZhou 121001, China.
6
Department of Urology surgery, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China. Electronic address: celion2004@126.com.
7
Department of Gastroenterology, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China. Electronic address: xhj_cn@126.com.
8
Department of Breast and Thyroid surgery, First Affiliated Hospital of Second Military Medical University, Shanghai 200433, China. Electronic address: lhy@smmu.edu.cn.

Abstract

Accumulative researches have demonstrated the critical functions of long non-coding RNAs (lncRNAs) in the progression of malignant tumors, including bladder cancer (BC). Our previous studies showed that lnc-DILC was an important tumor suppressor gene in both liver cancer and colorectal cancer. However, the role of lnc-DILC in BC remains to be elucidated. In the present study, we for first found that lnc-DILC was downregulated in human bladder cancer tissues. Lnc-DILC overexpression suppressed the proliferation, metastasis and expansion of bladder cancer stem cells (CSCs). Mechanically, lnc-DILC suppressed BC cells progression via STAT3 pathway. Special STAT3 inhibitor S3I-201 diminished the discrepancy of growth, metastasis and self-renewal ability between lnc-DILC-overexpression BC cells and their control cells, which further confirmed that STAT3 was acquired for lnc-DILC-disrupted BC cell growth, metastasis and self-renewal. Taken together, our results suggest that lnc-DILC is a novel bladder tumor suppressor and indicate that lnc-DILC inhibits BC progression via inactivating STAT3 signaling.

KEYWORDS:

Bladder cancer; Proliferation; STAT3; Self-renewal; lnc-DILC

PMID:
31176734
DOI:
10.1016/j.gene.2019.06.009

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